ライフサイエンスコーパス: coronary atherosclerosis

1 nts in the SIRCA (Study of Inherited Risk of Coronary Atherosclerosis).

2 with myocardial dysfunction and accelerated coronary atherosclerosis.

3 rating the benefit of imaging of subclinical coronary atherosclerosis.

4 ascular remodeling in the natural history of coronary atherosclerosis.

5 ther high volumes of exercise may accelerate coronary atherosclerosis.

6 endothelial function in patients with early coronary atherosclerosis.

7 assessment of changes in the full extent of coronary atherosclerosis.

8 vents in those with less extensive calcified coronary atherosclerosis.

9 Low LDL-C and SBP beneficially impact coronary atherosclerosis.

10 e associated with the slowest progression of coronary atherosclerosis.

11 of Th17 cells, is also associated with human coronary atherosclerosis.

12 which could potentially increase the risk of coronary atherosclerosis.

13 coronary calcium score (CCS) as a marker for coronary atherosclerosis.

14 and for the development of novel markers for coronary atherosclerosis.

15 no alternative to bypass surgery for severe coronary atherosclerosis.

16 strated the ability to reduce progression of coronary atherosclerosis.

17 hip between lipid changes and progression of coronary atherosclerosis.

18 inal subcutaneous fat, may be a correlate of coronary atherosclerosis.

19 eated patients demonstrated no regression of coronary atherosclerosis.

20 onship between lifelong exercise volumes and coronary atherosclerosis.

21 Inflammation also is associated with coronary atherosclerosis.

22 o significant decrease in the progression of coronary atherosclerosis.

23 nsistent with a protective role for CXCL5 in coronary atherosclerosis.

24 edictors of rapid progression of subclinical coronary atherosclerosis.

25 rolling for individual level risk factors of coronary atherosclerosis.

26 d fine particulate matter with the degree of coronary atherosclerosis.

27 oteasome inhibition is associated with early coronary atherosclerosis.

28 terol (LDL-C) levels and slow progression of coronary atherosclerosis.

29 lar remodeling is independent of preexisting coronary atherosclerosis.

30 igh traffic is associated with the degree of coronary atherosclerosis.

31 s that beta-blockers can slow progression of coronary atherosclerosis.

32 criteria for organ donors to include modest coronary atherosclerosis.

33 ol and plant sterols, resulting in premature coronary atherosclerosis.

34 an altered cardiac phenotype independent of coronary atherosclerosis.

35 rtension, and hypertension on progression of coronary atherosclerosis.

36 been reported to promote rapid regression of coronary atherosclerosis.

37 ammation and Th1-type cytokine production in coronary atherosclerosis.

38 arteriosclerotic Th1-type cytokines in human coronary atherosclerosis.

39 ons of psychosocial factors with subclinical coronary atherosclerosis.

40 hanisms of organismal aging and inflammatory coronary atherosclerosis.

41 er of the presence and extent of subclinical coronary atherosclerosis.

42 c subjects in the Study of Inherited Risk of Coronary Atherosclerosis.

43 t of plasma LDL-C levels and the severity of coronary atherosclerosis.

44 of reactive oxygen species, is a hallmark of coronary atherosclerosis.

45 mous senescent pathologic processes, such as coronary atherosclerosis.

46 eated with pravastatin showed progression of coronary atherosclerosis.

47 in patients with angiographically confirmed coronary atherosclerosis.

48 continues to revolutionize the treatment of coronary atherosclerosis.

49 brown adipose tissue (BAT) and the degree of coronary atherosclerosis.

50 e scintigraphy identifies predominantly mild coronary atherosclerosis.

51 ronary syndrome in patients with established coronary atherosclerosis.

52 in vasa vasorum neovascularization in early coronary atherosclerosis.

53 eptide that is crucial in the development of coronary atherosclerosis.

54 reflects an increased burden of subclinical coronary atherosclerosis.

55 in plasma cholesterol levels and early-onset coronary atherosclerosis.

56 f other risk factors, indicating preclinical coronary atherosclerosis.

57 finding in men who die suddenly with severe coronary atherosclerosis.

58 ation (CAC) allows noninvasive assessment of coronary atherosclerosis.

59 d against a control population with no known coronary atherosclerosis.

60 nction may play a role in the progression of coronary atherosclerosis.

61 HDL cholesterol concentrations, obesity, and coronary atherosclerosis.

62 lcification (CAC) is an imaging biomarker of coronary atherosclerosis.

63 e cells originated as SMCs in advanced human coronary atherosclerosis.

64 tic risk had a greater burden of subclinical coronary atherosclerosis.

65 , including surrogate markers of carotid and coronary atherosclerosis.

66 d models and their potential in the study of coronary atherosclerosis.

67 r regression or prevention of progression of coronary atherosclerosis.

68 ys in healthy participants, independently of coronary atherosclerosis.

69 in improvement or slowing of progression of coronary atherosclerosis.

70 and a history, or multiple risk factors, of coronary atherosclerosis.

71 (Lp-PLA(2)/PLA2G7) in human inflammation and coronary atherosclerosis.

72 ion in PLA2G7 is associated with subclinical coronary atherosclerosis.

73 .2-y progression of angiographically defined coronary atherosclerosis.

74 een BPA exposure and angiographically graded coronary atherosclerosis.

75 ically, to myocardial infarction in existing coronary atherosclerosis.

76 statin resulted in significant regression of coronary atherosclerosis.

77 to myocardial infarction in the presence of coronary atherosclerosis.

78 adulthood are independently associated with coronary atherosclerosis 2 decades later.

79 g adulthood is common and is associated with coronary atherosclerosis 20 years later.

80 ng history have increased risk of developing coronary atherosclerosis (21.2% vs. 12.3%), graft dysfun

81 Patients with coronary atherosclerosis also had highly proinflammatory

82 ation is associated with the pathogenesis of coronary atherosclerosis, although the mechanisms remain

83 the association of chronic HCV infection and coronary atherosclerosis among participants in the Multi

84 adipocytokines affect insulin resistance and coronary atherosclerosis among patients with RA.

85 en dietary macronutrients and progression of coronary atherosclerosis among postmenopausal women.

86 s associated with more extensive and diffuse coronary atherosclerosis and accelerated disease progres

87 f Lp-PLA2 is enhanced in patients with early coronary atherosclerosis and associated with local endot

88 s the focus away from obstructive epicardial coronary atherosclerosis and centers it on the microvasc

89 use is a new model of diet-induced occlusive coronary atherosclerosis and CHD (myocardial infarction,

90 sociated with development of both underlying coronary atherosclerosis and clinical events.

91 to limit the risk factors for development of coronary atherosclerosis and enable long-term survival a

92 PHT is associated with a worsening of coronary atherosclerosis and exacerbation of the profile

93 tion is an early stage in the development of coronary atherosclerosis and has been implicated in the

94 r imaging has made advances toward targeting coronary atherosclerosis and heart failure.

95 ysis were performed in 15 patients with mild coronary atherosclerosis and in 15 control subjects.

96 a were detected in a subset of patients with coronary atherosclerosis and in referent outpatients of

97 ved from cigarette smoke is known to promote coronary atherosclerosis and increase the likelihood of

98 intima-media thickness (CIMT) is a marker of coronary atherosclerosis and independently predicts card

99 In classic Fabry patients, accelerated coronary atherosclerosis and left ventricular hypertroph

100 ol, a key stress hormone, is associated with coronary atherosclerosis and may accentuate structural a

101 nd balanced ischemia from diffuse epicardial coronary atherosclerosis and microvascular dysfunction.

102 ry calcification (CAC) accurately identifies coronary atherosclerosis and might improve prediction of

103 cal CAD, almost three-fourths had high-grade coronary atherosclerosis and more than half had multives

104 Coronary atherosclerosis and myocardial infarction in po

105 eciated, contributing to the pathogenesis of coronary atherosclerosis and myocardial infarction.

106 provide new opportunities for investigating coronary atherosclerosis and stent healing and for ident

107 ortality that is mediated by the presence of coronary atherosclerosis and systemic inflammation can b

108 tion (CAC) reflects the anatomic presence of coronary atherosclerosis and the relative burden of coro

109 hronic vascular inflammation predisposing to coronary atherosclerosis and to thrombosis.

110 ter adjusting for the extent and severity of coronary atherosclerosis and traditional risk factors.

111 he role of low ESS in the natural history of coronary atherosclerosis and vascular remodeling and ind

112 ptoms increase progression in other types of coronary atherosclerosis and whether aggressive lipid lo

113 he pattern of arterial remodeling, extent of coronary atherosclerosis, and disease progression was co

114 eletal development, osteoblastic metastasis, coronary atherosclerosis, and other human diseases.

115 tein cholesterol (LDL-C) levels, severity of coronary atherosclerosis, and response to statin therapy

116 enal function is an important determinant of coronary atherosclerosis, and serum cystatin C is a nove

117 l insufficiency, a greater overall burden of coronary atherosclerosis, and suboptimal final angiograp

118 tivity, the importance of these processes to coronary atherosclerosis, and the advantages and challen

119 elial shear stress in the natural history of coronary atherosclerosis, and to propose an individualiz

120 ffects of these categories on progression of coronary atherosclerosis are unknown.

121 e findings challenge our traditional view of coronary atherosclerosis as a segmental or localized dis

122 health (ICH) and the presence of subclinical coronary atherosclerosis as assessed by coronary artery

123 FLD, traditional risk factors, and extent of coronary atherosclerosis as independent variables.

124 intervals produced significant regression of coronary atherosclerosis as measured by IVUS.

125 ld perfusion defects of early nonobstructive coronary atherosclerosis as the basis for intense lifest

126 noninvasive assessment of early or advanced coronary atherosclerosis as the basis for invasive proce

127 The amount of coronary atherosclerosis, as can be extrapolated from CT

128 ensive statin regimens on the progression of coronary atherosclerosis, as well as to assess their saf

129 ering on cardiovascular events, had baseline coronary atherosclerosis assessed by coronary artery cal

130 elationship between gender and the extent of coronary atherosclerosis assessed by intravascular ultra

131 y was associated with reduced progression of coronary atherosclerosis assessed by quantitative corona

132 ed tomography has the advantage of detecting coronary atherosclerosis at its earliest stages and also

133 ing symptomatic patients with nonobstructive coronary atherosclerosis because current diagnostic crit

134 0(-6), 10(-5), 10(-4) M) in 29 patients with coronary atherosclerosis before and 18 +/- 5.2 months af

135 This study demonstrates that coronary atherosclerosis begins at a young age and that

136 In patients with established coronary atherosclerosis, BMI, as well as CRP and number

137 ncentration was an independent predictor for coronary atherosclerosis burden (P=0.02) and predicted l

138 Increased TMAO concentrations correlate with coronary atherosclerosis burden and may associate with l

139 ectional relationship between serum TMAO and coronary atherosclerosis burden in a separate CKD cohort

140 d coronary-artery calcification, a marker of coronary atherosclerosis burden.

141 Overall, 95% had coronary atherosclerosis, but only 39% had 1 or more ste

142 e increased the risk of advanced subclinical coronary atherosclerosis by 36% (P=8.3x10(-25)).

143 Secondary outcomes included an assessment of coronary atherosclerosis by cardiac computed tomography

144 etic patients for either (A) the presence of coronary atherosclerosis by imaging of coronary calcific

145 assessed whether rosuvastatin could regress coronary atherosclerosis by intravascular ultrasound and

146 infarctions and features of infarct-related coronary atherosclerosis by serial noninvasive molecular

147 nstable angina) in patients with and without coronary atherosclerosis (CAD).

148 These findings suggest that coronary atherosclerosis can be avoided in most people b

149 CAC as a sign of subclinical coronary atherosclerosis can noninvasively be detected b

150 We used a model of porcine coronary atherosclerosis characterized by smooth muscle

151 ject, which allows rigorous ascertainment of coronary atherosclerosis, clinical CAD, and diabetes.

152 sive medical therapy to treat the widespread coronary atherosclerosis commonly seen in patients with

153 a significantly lower rate of progression of coronary atherosclerosis compared with glimepiride.

154 ent with atorvastatin reduced progression of coronary atherosclerosis compared with pravastatin.

155 centage of EPCs express OCN in patients with coronary atherosclerosis compared with subjects with nor

156 tant PAD harbor more extensive and calcified coronary atherosclerosis, constrictive arterial remodeli

157 ether a direct influence of beta-blockers on coronary atherosclerosis contributes to reduced recurren

158 ic function (early relaxation velocity), and coronary atherosclerosis (coronary artery plaque volume)

159 The influence of donor-transmitted coronary atherosclerosis (DA) on plaque progression duri

160 Coronary atherosclerosis develops slowly over decades bu

161 al dysfunction, n = 21) versus 2 groups with coronary atherosclerosis-early coronary atherosclerosis

162 Type 1 diabetes is associated with increased coronary atherosclerosis, especially in women, even thou

163 In addition to inhibiting coronary atherosclerosis, estrogen may also have protect

164 an important predictive measure of clinical coronary atherosclerosis events in middle-aged and elder

165 0 HIV-infected participants with subclinical coronary atherosclerosis, evidence of arterial inflammat

166 RBI(-/-) has been shown to develop occlusive coronary atherosclerosis followed by myocardial infarcti

167 tify EPCs, we examined whether patients with coronary atherosclerosis had increases in the percentage

168 ontrol patients, patients with early or late coronary atherosclerosis had significant increases (appr

169 e of this phenotypic switch by SMCs in human coronary atherosclerosis has not been determined.

170 olipoprotein A1 (apoA1) levels and premature coronary atherosclerosis, has led to the hypothesis that

171 Previous studies of native coronary atherosclerosis have demonstrated associations

172 y was designed to test whether patients with coronary atherosclerosis have increases in circulating e

173 ents; however, the effects of these drugs on coronary atherosclerosis have not been evaluated.

174 Among the autopsied group with severe coronary atherosclerosis, HDL cholesterol was higher and

175 oth the prevention and medical management of coronary atherosclerosis; however, additional or alterna

176 The results suggest that, in human coronary atherosclerosis, IL-8 is an important mediator

177 Detection of subclinical carotid or coronary atherosclerosis improves risk predictions and r

178 polymorphisms and the degree of subclinical coronary atherosclerosis in 7798 participants from 6 stu

179 ased intracellular oxidative stress in human coronary atherosclerosis in a cell-specific manner and t

180 We sought to compare the prevalence of coronary atherosclerosis in a cohort of middle-age Afric

181 xamined the association between diabetes and coronary atherosclerosis in a geographically defined aut

182 t of a large lipid-lowering trial addressing coronary atherosclerosis in a specific diabetic populati

183 It may therefore be valuable for diagnosing coronary atherosclerosis in acute myocardial infarction

184 Obesity is associated with accelerated coronary atherosclerosis in adolescent and young adult m

185 ated with obesity and enhanced complexity of coronary atherosclerosis in adults.

186 nt of AGEs in the development of accelerated coronary atherosclerosis in diabetes.

187 h darapladib reduced development of advanced coronary atherosclerosis in diabetic and hypercholestero

188 Multiple pathways contribute to accelerated coronary atherosclerosis in diabetics, including increas

189 Early coronary atherosclerosis in humans is characterized by l

190 arkers of inflammation and are predictive of coronary atherosclerosis in humans, independent of CRP.

191 function as markers-and perhaps mediators-of coronary atherosclerosis in humans.

192 of Lp(a) are an independent risk factor for coronary atherosclerosis in individuals of African desce

193 y food resources may slow the development of coronary atherosclerosis in middle-aged and older adults

194 The prevalence of coronary atherosclerosis in middle-aged blacks and white

195 lysis was to characterize the progression of coronary atherosclerosis in patients with concomitant pe

196 ncreased and associated with the severity of coronary atherosclerosis in patients with RA.

197 Metformin may protect against coronary atherosclerosis in prediabetes and early diabet

198 ensive statin therapy reduces progression of coronary atherosclerosis in proportion to achieved LDL-C

199 ascular outcomes and slow the progression of coronary atherosclerosis in proportion to their ability

200 scular risk factors and advanced subclinical coronary atherosclerosis in risk stratification.

201 tracellular components associated with human coronary atherosclerosis in situ.

202 o determine 1) the prevalence of subclinical coronary atherosclerosis in SSc and 2) serum piHDL level

203 inhibition with evolocumab on progression of coronary atherosclerosis in statin-treated patients.

204 y or manifest the progression to subclinical coronary atherosclerosis in the absence of clinical CHD.

205 CA1 genotypes are potential risk factors for coronary atherosclerosis in the general population.

206 rmine HDL-C and apoA1 levels and the risk of coronary atherosclerosis in the general population.

207 4-slice CTCA in detecting and characterizing coronary atherosclerosis in these patients.

208 The extent of coronary atherosclerosis in this patient set strongly co

209 erial inflammation and achieve regression of coronary atherosclerosis in this population.

210 esterone acetate affected the progression of coronary atherosclerosis in women with established disea

211 pproximately 15% of the effect of obesity on coronary atherosclerosis in young men.

212 BMI was not associated with coronary atherosclerosis in young women although there w

213 ary artery calcification (CAC), a measure of coronary atherosclerosis, in the Multi-Ethnic Study of A

214 h MetSyn and HOMA index were associated with coronary atherosclerosis independent of established risk

215 Coronary atherosclerosis is a chronic inflammatory disea

216 fusion of rHDL containing AIM, regression of coronary atherosclerosis is accompanied by reverse remod

217 Coronary atherosclerosis is associated with endothelial

218 o test the hypothesis that the prevalence of coronary atherosclerosis is greater among diabetic than

219 Prevalence of subclinical coronary atherosclerosis is greater in patients with SSc

220 The prevalence of subclinical coronary atherosclerosis is increased in patients with r

221 , and yet several studies have reported that coronary atherosclerosis is less prevalent in blacks tha

222 The most favorable rate of progression of coronary atherosclerosis is observed in patients whose B

223 artery bypass grafting were studied because coronary atherosclerosis is recognized as a Th1-type inf

224 n, a marker for the presence and quantity of coronary atherosclerosis, is higher in US whites than bl

225 le in chronic inflammatory diseases, such as coronary atherosclerosis, is not well defined.

226 ationship was observed between the burden of coronary atherosclerosis, its progression, and adverse c

227 vegetables (F/V) during young adulthood and coronary atherosclerosis later in life is unclear.

228 In patients with angiographically confirmed coronary atherosclerosis, leptin is a novel predictor of

229 Therefore, the burden of coronary atherosclerosis may be closer among younger per

230 gated the hypothesis that baseline calcified coronary atherosclerosis may determine cardiovascular di

231 ective: To assess the burden of asymptomatic coronary atherosclerosis measured by coronary artery cal

232 We evaluated correlates of coronary atherosclerosis, measured by coronary artery ca

233 We aimed to compare prevalences of coronary atherosclerosis, measured with coronary artery

234 of this study was to quantify the effects of coronary atherosclerosis morphology and extent on myocar

235 sease (CHD): hypercholesterolemia, occlusive coronary atherosclerosis, myocardial infarctions, cardia

236 Activity was higher in patients with coronary atherosclerosis (n = 106) versus control subjec

237 Patients with pre-existing donor coronary atherosclerosis (n = 35) or with acute rejectio

238 1.4% men) and the Study of Inherited Risk of Coronary Atherosclerosis (N = 803 nondiabetic subjects,

239 2 groups with coronary atherosclerosis-early coronary atherosclerosis (normal coronary arteries but w

240 For the primary end point, progression of coronary atherosclerosis occurred in the pravastatin gro

241 The burden of coronary atherosclerosis on computed tomography angiogra

242 ct detrimental effects on the progression of coronary atherosclerosis, on the occurrence of myocardia

243 trials reported no benefit of torcetrapib on coronary atherosclerosis or carotid artery intimal media

244 ion between the genotypes and progression of coronary atherosclerosis or clinical events was detected

245 risk factors, possibly reflecting developing coronary atherosclerosis or preclinical CAD.

246 ficacy trials of MLu PT for the treatment of coronary atherosclerosis or vulnerable plaque.

247 en demonstrated in patients with established coronary atherosclerosis or with risk factors in respons

248 stinctly contribute to either development of coronary atherosclerosis or, specifically, to myocardial

249 as positively associated with progression of coronary atherosclerosis (P-trend < 0.05).

250 r increases were noted in the early and late coronary atherosclerosis patients in the percentage of C

251 CT has been used to track the progression of coronary atherosclerosis periodically.

252 ols, SSc patients had a higher prevalence of coronary atherosclerosis, peripheral vascular disease, a

253 Recurrent Events trial, the Air Force/Texas Coronary Atherosclerosis Prevention studies, and Long-te

254 ong 5569 participants in the Air Force/Texas Coronary Atherosclerosis Prevention Study (AFCAPS/TexCAP

255 ronary Prevention Study, the Air Force/Texas Coronary Atherosclerosis Prevention Study, the Cholester

256 Our goal was to characterize coronary atherosclerosis progression and arterial remode

257 The impact of concomitant PAD on coronary atherosclerosis progression in patients with co

258 he processes underlying the heterogeneity of coronary atherosclerosis progression in relation to the

259 ated to greater CVD risk in older adults and coronary atherosclerosis progression in women with IHD.

260 cardiomyocytes, cardiac fibrosis as well as coronary atherosclerosis progression.

261 es in immunosuppressive therapy, accelerated coronary atherosclerosis remains a major problem in the

262 nti-inflammatory drugs on the development of coronary atherosclerosis remains essentially unknown.

263 its ability to predict sustained absence of coronary atherosclerosis remains unknown.

264 e is a locus on chromosome 2 that influences coronary atherosclerosis risk.

265 would 1) predict progression of subclinical coronary atherosclerosis (SCA) and 2) be a stronger pred

266 ndrogenic activity-possibly a determinant of coronary atherosclerosis-several studies have explored t

267 th endothelial dysfunction, n = 22) and late coronary atherosclerosis (severe, multivessel coronary a

268 CL5 and molecular phenotypes associated with coronary atherosclerosis severity in patients at least 6

269 Classifications of coronary atherosclerosis severity were determined prior

270 the general population have a prevalence of coronary atherosclerosis similar to whites.

271 and stacked discoidal particles), occlusive coronary atherosclerosis, spontaneous myocardial infarct

272 esponse to statin therapy in the Lipoprotein Coronary Atherosclerosis Study (LCAS) population.

273 o fluvastatin therapy in the Lipoprotein and Coronary Atherosclerosis Study (LCAS) population.

274 participants in the prospective Lipoprotein Coronary Atherosclerosis Study (LCAS), and determined th

275 dhood obesity with obesity and complexity of coronary atherosclerosis (SYNTAX score) in a cohort of 3

276 e hypertensive rat model of male-predominant coronary atherosclerosis, Tg25.

277 is more strongly associated with subclinical coronary atherosclerosis than a parental history of prem

278 in the United States had a higher burden of coronary atherosclerosis than Japanese men, but the ethn

279 er burden of the excess cholesterol in human coronary atherosclerosis than previously known, in part,

280 A disease process other than coronary atherosclerosis that explained the presenting s

281 dysfunction is considered an early phase of coronary atherosclerosis, there is a paucity of informat

282 ease is associated with advanced subclinical coronary atherosclerosis throughout the life-course.

283 Allograft coronary atherosclerosis (TxCAD) is the leading cause of

284 ured by ELISA in the plasma of patients with coronary atherosclerosis undergoing cardiac catheterizat

285 importance of genetic factors in subclinical coronary atherosclerosis variation as measured by CAC qu

286 advanced atherosclerosis featuring occlusive coronary atherosclerosis, vulnerable plaque, and prematu

287 The prevalence of any coronary atherosclerosis was 8.5% (95% CI, 7.6%-9.4%); s

288 eart Association guidelines, and subclinical coronary atherosclerosis was assessed by computed tomogr

289 Coronary atherosclerosis was assessed by coronary artery

290 Coronary atherosclerosis was identified in 68% and syste

291 The burden and progression of coronary atherosclerosis was investigated in 3,479 patie

292 lerosis was 8.5% (95% CI, 7.6%-9.4%); severe coronary atherosclerosis was present in 2.3% (95% CI, 1.

293 tin therapy is associated with regression of coronary atherosclerosis when LDL-C is substantially red

294 c predispositions promote the development of coronary atherosclerosis whereas others lead to myocardi

295 ntake is associated with less progression of coronary atherosclerosis, whereas carbohydrate intake is

296 puted tomography is a noninvasive measure of coronary atherosclerosis, which underlies most cases of

297 Coronary atherosclerosis with occlusive thrombosis is th

298 Acute coronary syndromes arise from coronary atherosclerosis with superimposed thrombosis.

299 disease process caused by the development of coronary atherosclerosis, with downstream effects on the

300 s likely to contribute to the development of coronary atherosclerosis, yet the factors that regulate